Temperature management in CPB

History-

Lewis and taufic used hypothermia and inflow occlusion for repair of ASD

Sealy used hypothermia for CPB Circuit for intracardiac repair.

Physiology of Hypothermia

Normal homeostatic mechanism with exposure to cold is – activation of thermoreceptor in brain -> hypothalamic sympathetic nerve stimulation

Hence,

1. Vasoconstriction of skin venues

2. Vasodilation of skeletal muscle venules -> increase muscular activity by tensing and shivering

3. Endocrine system is activated and O2 consumption is increased

4. HR/ CO/BP are elevated

Rationale of use of Hypothermia in CPB-

1. Organ protection and safety margin in CPB

2. By decreasing metabolic rate and O2 consumption.

3. Preserves high energy phosphate stores

4. Decrease excitatory neurotransmitter release as increase in neurotransmitter like glutaraldehyde opens up calcium channels and calcium dependent caspases activation and cell death.

4. Q10 — increase or decrease in temperature dependent enzymatic reaction per 10 degree C change in temperature.

Most reactions including O2 consumption have a Q10 of 2-3.

5. In CPB it helps in

* Lowering pump flows for better visualisation of surgical field

* Better myocardial protection- by decreasing temperature

* Less blood trauma- due to decrease pump flow and hemodilution

* Better organ protection

Acid base alteration with temperature change

* With increase in temperature – PCO2 decreases

Decrease in temperature – PCO2 increase

* Major buffering system responsible for the constant relation of blood and tissue fluid pH to neutral pH with temperature change is the imidazole moiety of amino acid histidine which is commonly found in body proteins.

* PKa of histidine is nearly 7.0

* Alpha = ratio of unprotonated histidine imidazole group to H+ ion

Alpha stat — CO2 is constant  and pH changes as per the body temperature. In otherwors CO2 is not added to the system during cooling.

PH stat— pH remains constant and CO2 is added to maintain PaCO2 and a pH of 7.4

( Alpha and pH stat are important to maintain the intracellular enzyme system as most of the enzymatic reaction are pH dependant)

* With response to hypothermia-

Cerebral blood flow decreases ut with alpha stat strategy this decrease in CBF is adequate for maintaining metabolic demand as metabolic demand is also decreased due to hypothermia. Therefore alpha stat strategy will result in decreased cerebral blood flow than the pH stat strategy ( the response of cerebral blood flow is preserved with changes in PaCO2 in a alpha stat strategy.

In alpha stat strategy, hypocarbia shifts the oxygen hemoglobin dissociation curve to the left thus decreasing O2 unloading however more O2 is dissolved in blood in hypothermia cancelling each other.

Studies have demonstrated that post op neurological and neuropsychological outcome is better with alpha stat strategy.

In pH stat — Cerebral blood flow is increased and thus exposed to a greater load of –

Microemboli

Cerebral edema

High intracranial pressure

On the other hand, it is suggested that increase in cerebral blood flow may be helpful in improving cerebral cooling before the onset of circulatory arrest. And an increased amount of blood is supplied to the deep brain structures like thalamus or midbrain or cerebellum.

Crossover strategy—PH strategy for first 10 minutes of cooling to provide maximal cerebral suppression followed by alpha stat to remove severe acidosis that accumulate during profound hypothermia.

In paediatric patients – Cerebral cooling is problematic and it appears that addition of CO2 during cooling enhances cerebral perfusion and improves cerebral metabolic recovery.

Overall, in adult the primary cause of neurological injury is probably due to embolisation hence decrease CBF (alpha stat strategy) is more beneficial where as in paediatric population hypo perfusion is the primary mechanism (hence pH stat strategy) with increase in CBF is beneficial.

Effect of Hypothermia on other organs

1. Peripheries- Decrease in blood flow to all organs-

Skeletal muscles/ Extremities—> Kidney—> Splanchnic bed —> Heart ——> Brain

( In this order)

2. Heart- With cooling HR increases but contractility remains stable/ may actually increase. Dysarrhythmia becomes more prominent in  hypothermia because of – PVC. AV block, AF, VF, Asystole- due to electrolyte imbalance, uneven cooling and autonomic imbalance

3. Lungs- Progressive decrease in ventilation with cooling. Physiological and anatomical dead space increase . Gas exchange is unaffected.

4. Kidney- Kidney shows the largest proportional decrease in blood flow of all organs. Increases renal vascular resistance. Tubular transport of Na+/Cl_/water decreased. Tubular reabsorption is decreased. Glucose absorption is decreased and glucose is found in urine.

5. Liver- Hepatic arterial blood flow is decreased. Decrease in metabolic and excretory function  of liver. With rewarming, hepatic efficiency reverts to normal.

6. Metabolic / Endocrine- Marked hyperglycaemia. Insulin production is decreased. Glycogenolysis and gluconeogenesis is increased.

Hypothermia – decreased free water clearance and causes a decrease in plasma K+ and increase in osmolality.

Increase in blood viscosity due to fluid shifts , loss of plasma volume from capillary leak, cell swelling. Hematocrit increase but RBC volume unchanged. Rouleaux formation increase. Cause thrombocytopenia.

Deep hypothermia cause massive release of cathecolamines.

Complement activation or increase bradykinin or increase neutrophil activation due to hypothermia.

Use of hypothermia

* In most cardiac surgeries hypothermia  (>25 C ) is used for its protective role

* By coronary perfusion with cold cardioplegia solution or topical application of air ice slush or cold pericardial lavage

* Classification of hypothermia-

Mild- 32-36

Moderate- 28-32

Severe- 28-18

Deep – <18

Systemic O2 consumption (VO2) is reduced by 50% for every 7 degree C reduction in core temperature below normothermia.

 

DNB CTVS Questions- December 2010

DECEMBER 2010  

PAPER I
1.Enumerate deleterious effects of hypothermia on organ systems during      cardiopulmonary bypass. 10
2. Development of aortic arch with brief discussion on vascular ring. 10
3.  Classification o f mediastinum. Enumerate common tumours of each area. 10
4. process and criteria of sample size selection for a clinical study. 10
5. draw a labeled diagram and discuss the circulation changes that occur at the time of birth and their pathophysiological significance. 10
6. discuss in brief with labeled diagrams various surgical modalities in the management of  atrial fibrillation. 10
7.  enumerate neuroprotective strategies and their use in various surgical operations. Highlight use of one strategy of your choice. 10
8. diagnosis and management of heparin induced thrombocytopenia. 10
9. development of left superior vena cava and its implications during cardiac surgery. 10
10. diagnosis and cardiovascular manifestations of Marfan’s disease. 10
DECEMBER 2010   PAPER II
1. Aetiopathogenesis of thoracic outlet syndrome. 10
2. Presentation and surgical management of sequestration of lung. 10
3. Classification and surgical management (in brief) of tricuspid atresia.10
4. Classification and surgical management (in brief) of truncus arteriosus. 10
5. Pulmonary vascular disease and its investigation and grading.10
6. Mitral Valve Replacement – advantages of total chordal preservation and comparison with other techniques. 10
7. Coronary artery bypass- comparison of radial, saphenous vein and internal thoracic artery in term of histopathology and long term outcome. 10
8. Classification of thoraco-abdominal aortic aneurysms and role of endovascular interventions in their management. 10
9. Explain with diagram different surgical procedures for the management of small aortic root and comparative chart of their advantages and disadvantages. 10
10. Basic component and modifications of myocardial protection. 10

DECEMBER 2010   PAPER III
1. Cell sources for cardiac tissue engineering. 10
2. Centrifugal pump: advantages and disadvantages of its use in assisted circulation. 10
3. “No flow” phenomenon in myocardial ischemia.10
4. Computed tomography in re-operative cardiac surgeries and its role in pre operative planning and surgical guidance. 10
5. Role of hybrid operative interventions in cardiovascular surgery. 10
6. Current status  of cardiac transplantation. 10
7. Power source, current status and future development of artificial heart. 10
8. Newer oral anticoagulants and their role in DVT, AF, and Cardiological interventions. 10
9. Advantages and disadvantages of Virtual bronchoscopy. 10
10. Percutaneous valve implantation- in various positions, evolutions and future direction. 10